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Degenhardt, K.* ; Wagner, J.* ; Skodras, A.* ; Candlish, M.* ; Koppelmann, A.J.* ; Wild, K.* ; Maxwell, R.* ; Rotermund, C.* ; von Zweydorf, F.* ; Gloeckner, C.J.* ; Davies, H.A.* ; Madine, J.* ; Del Turco, D.* ; Feederle, R. ; Lashley, T.* ; Deller, T.* ; Kahle, P.* ; Hefendehl, J.K.* ; Jucker, M.* ; Neher, J.J.*

Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice.

Proc. Natl. Acad. Sci. U.S.A. 117, 23925-23931 (2020)
DOI Verlagsversion bestellen
: Verlagsversion online verfügbar 05/2021
Medin is the most common amyloid known in humans, as it can be found in blood vessels of the upper body in virtually everybody over 50 years of age. However, it remains unknown whether deposition of Medin plays a causal role in age-related vascular dysfunction. We now report that aggregates of Medin also develop in the aorta and brain vasculature of wild-type mice in an age-dependent manner. Strikingly, genetic deficiency of the Medin precursor protein, MFG-E8, eliminates not only vascular aggregates but also prevents age-associated decline of cerebrovascular function in mice. Given the prevalence of Medin aggregates in the general population and its role in vascular dysfunction with aging, targeting Medin may become a novel approach to sustain healthy aging.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Medin ; Mfg-e8 ; Cerebrovascular Dysfunction ; Aging ; Amyloid; Smooth-muscle-cells; Mouse Model; A-beta; Blood-flow; Amyloidosis; Growth; Mfg-e8; Vasculature; Dementia; Integrin
ISSN (print) / ISBN 0027-8424
e-ISSN 1091-6490
Quellenangaben Band: 117, Heft: 38, Seiten: 23925-23931 Artikelnummer: , Supplement: ,
Verlag National Academy of Sciences
Verlagsort 2101 Constitution Ave Nw, Washington, Dc 20418 Usa
Begutachtungsstatus Peer reviewed
Institut(e) Monoclonal Antibody (IDO-MAB)
Förderungen DFG
British Heart Foundation
German Research Foundation (DFG)